Clinical reports of the immediate post-spinal cord injury (SCI) phase indicate that gastrointestinal stasis, or ileus, results in complications from aspiration and reflux. Gastric feeding intolerance necessitates aggressive total parenteral nutrition and occasionally invasive and Gl surgical intervention (with associated risk of complications) for the maintenance of a positive energy and nitrogen balance. The resultant risk of aspiration that accompanies severe and prolonged gastric stasis requires intensive management of the airway and is a significant cause of post-trauma morbidity and mortality. Various degrees of this syndrome may continue long after stabilization from the initial trauma thus having profound negative effects on the patient's quality of life after SCI. The scope of the project is to use a high thoracic (spinal level T3) model of spinal contusion injury using established techniques by the PI to the study of post-SCI gastric stasis. Gastric motility and emptying is heavily mediated by parasympathetic reflexes that incorporate general visceral afferent input to the medulla via the vagus nerve. Medulary control of gastric motility returns to the stomach via vagal efferents. This vago-vagal reflex remains anatomically intact in the SCI patient. However, the post-injury gastric morbidity suggests that a spinally-mediated input to the medulla is disrupted, resulting in an excitation of well documented medullary circuits that produce a spastic gastroparesis similar to truncal vagotomy. Use of a high thoracic injury model will maximize the reduction in spinal relays for gastric visceral afferent information to the DVC. In so doing the following Specific Aims will be addressed 1) T3 contusion lesion will produce a spastic gastric paralysis (i.e., reduced gastric emptying, elastance, and motility);2) Identify that the loss of ascending spinosolitary inputs is the basis for alterations in gastric reflexes after SCI;3) Identify the projections and neurochemical phenotypes of the ascending spinosolitary fibers and the brainstem neurons upon which they act;4) After mild to moderate SCI, post-injury gastric stasis will demonstrate anatomical recovery overtime. The long term goal of this laboratory is to establish a model of post-SCI alterations in gastrointestinal function that encompasses the entire length of the Gl tract in order to alleviate Gl dysfunction in human SCI patients. The Pi's research on distal gut (bowel) eliminative reflexes after SCI, coupled with the Co-l's research on brainstem regulation of gastric function is clearly complementary.